Genetic Regulator Identified as Possible Treatment Target in Melanoma

Rutgers Cancer Institute of New Jersey research published

April 3, 2014

New Brunswick, N.J. – Research from Rutgers Cancer Institute of New Jersey shows that the RUNX2 protein, which regulates the transcription of genetic messages responsible for the different functions of cells, may play a role in melanoma cell growth and spread and could serve as a therapeutic target for the disease.

Abnormal and uncontrolled production of this class of proteins, known as transcription factors, allow for cells to bypass growth control mechanisms and to develop characteristics necessary for invading surrounding tissues. Some transcription factors already have been identified as playing a role in melanoma development. These discoveries come into a favorable context of new drugs against transcription factors being tested in clinical trials. In the study, published in the current online edition of Cancer Letters (doi.org/10.1016/j.canlet.2014.03.011), senior author Karine Cohen-Solal, PhD, and colleagues show for the first time that the RUNX2 transcription factor could also serve as a possible treatment target for melanoma.

This latest research shows deviant messaging translated through RUNX2 may result in melanoma growth, migration and invasion. In order to further understand the impact of such abnormal messaging, investigators artificially reduced the amount of RUNX2 in melanoma cells through a genetic approach. As a result, reduced abilities for cell growth, migration and invasion were found.

“Successful efforts to render transcription factors ‘drugable’ by interfering with different aspects of their transcriptional activity make this class of proteins attractive targets for therapy,” says Dr. Cohen-Solal, a researcher at the Cancer Institute and an assistant professor of medicine at Rutgers Robert Wood Johnson Medical School. “Exploring the role of RUNX2 in the development of melanoma is likely to reveal new mechanisms driving melanoma progression and identify a target for novel anti-melanoma agents, thereby opening new avenues for the treatment of this disease.”

Along with Cohen-Solal, the author team consists of Rajeev K. Boregowda, Oyenike O. Olabisi, Walid Abushahba, Byeong-Seon Jeong, and Keneshia K. Haenssen, all Cancer Institute and Robert Wood Johnson Medical School; Wenjin Chen, Cancer Institute; Marina Chekmareva, Cancer Institute and Robert Wood Johnson University Hospital; Ahmed Lasfar, Ernest Mario School of Pharmacy at Rutgers University; and David J. Foran, and James S. Goydos, both Cancer Institute and Robert Wood Johnson Medical School.

The work was supported in part by the New Jersey Commission on Cancer Research (09-1143-CCR-EO – Cohen-Solal), National Cancer Institute (Cancer Center Support Grant CCSG P30CA072720 and 1R01CA149627-01 - Goydos), American Cancer Society (11683-RSG-09-087-01-TBE - Cohen-Solal), National Institutes of Health (K12 GM093854-01, 5R01CA156386-08, 5R01CA161375-02) and the National Library of Medicine (5R01LM011119-03 – Foran).

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